ArticleScientific reports2017
Rogdi Defines GABAergic Control of a Wake-promoting Dopaminergic Pathway to Sustain Sleep in Drosophila.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 18 citations in OpenAlex.
- A cell-autonomous role for the vitamin B6 metabolism geneJournal of neurogenetics · 2025Article
- The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.Scientific reports · 2024Article
- Genome-wide association in Drosophila identifies a role for Piezo and Proc-R in sleep latency.Scientific reports · 2024Article
- Perampanel effectiveness in treating ROGDI-related Kohlschütter-Tönz syndrome: first reported case in China and literature review.BMC medical genomics · 2023Review
- Astrocytic GABA transporter controls sleep by modulating GABAergic signaling in Drosophila circadian neurons.Current biology : CB · 2022Article
- Metabolic flux from the Krebs cycle to glutamate transmission tunes a neural brake on seizure onset.PLoS genetics · 2021Article
- Receptors and Channels Associated with Alcohol Use: Contributions fromNeuroscience insights · 2021Review
- Article
- Sleep, brain vascular health and ageing.GeroScience · 2020Review
- Cleavage of human tau at Asp421 inhibits hyperphosphorylated tau induced pathology in a Drosophila model.Scientific reports · 2020Article
- An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins.Journal of visualized experiments : JoVE · 2018Article
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Authors and funding
12 authors at 4 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Kohlschutter-Tönz syndrome (KTS) is a rare genetic disorder with neurological dysfunctions including seizure and intellectual impairment. Mutations at the Rogdi locus have been linked to development of KTS, yet the underlying mechanisms remain elusive. Here we demonstrate that a Drosophila homolog of Rogdi acts as a novel sleep-promoting factor by supporting a specific subset of gamma-aminobutyric acid (GABA) transmission. Rogdi mutant flies displayed insomnia-like behaviors accompanied by sleep fragmentation and delay in sleep initiation. The sleep suppression phenotypes were rescued by sustaining GABAergic transmission primarily via metabotropic GABA receptors or by blocking wake-promoting dopaminergic pathways. Transgenic rescue further mapped GABAergic neurons as a cell-autonomous locus important for Rogdi-dependent sleep, implying metabotropic GABA transmission upstream of the dopaminergic inhibition of sleep. Consistently, an agonist specific to metabotropic but not ionotropic GABA receptors titrated the wake-promoting effects of dopaminergic neuron excitation. Taken together, these data provide the first genetic evidence that implicates Rogdi in sleep regulation via GABAergic control of dopaminergic signaling. Given the strong relevance of GABA to epilepsy, we propose that similar mechanisms might underlie the neural pathogenesis of Rogdi-associated KTS.
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